New Study Uncovers the Impact of Junk Food on Brain Function and Behavior
A game-changing article in Neuropharmacology has revealed the far-reaching consequences of high-calorie, sugary, and fatty “junk-food” diets for brain function and behavior. It was found that these diets not only change neural pathways but also influence food-seeking behaviours, especially in individuals prone to obesity. This discovery can have important implications for comprehending obesity and developing ways to solve it.
Understanding Reward Center of Brain
With increasing obesity globally, it is imperative to understand how calorie-dense diet affects brain function. Previous studies have indicated that such a diet could alter the functioning of brain reward centers especially nucleus accumbens (Smith et al., 2010). This significant region takes part in processing pleasurable stimuli and reinforcement by releasing dopamine which influences motivation, pleasure, and reward-seeking behaviors.
However, there is limited information concerning how changes in the nucleus accumbens resulting from dietary influences vary between obesity-prone individuals and those who are resistant. The purpose of this study was to know more about those differences while exploring how junk-food consumption followed by deprivation alters food-seeking behavior as well as plasticity within the nerve cells.
Methodology and Experiments: The Study
To achieve this goal obese-prone male rats were selectively bred; they were divided into three groups: rats that were fed on standard laboratory chow, special junk food access group and junk food with subsequent deprivation that had only standard lab chow access. The junk-food diet consisted of a mash made from Ruffle potato chips, Chips Ahoy cookies, Nesquik, Jiff peanut butter mixed with normal lab chow meant to be a mimicry of human high calorie high fat diet.
The behavioral experiments involved Pavlovian conditioning, instrumental training as well as testing aimed at assessing motivation for seeking food. These experiments assessed how motivated the rats were by counting numbers of times a lever was pressed when trying to get food pellets. Additionally, free consumption tests measured how much food the rats consumed when given free access to pellets, both under normal conditions and after a period of food restriction.
Key Findings: Behavioral and Neural Changes
The research demonstrated that there were different behavioral changes specific to the junk-food diet in obesity-prone rats. All rats behaved similarly during conditioned reinforcement experiments revealing a similar motivation to work for presentation of a food cue.
Behavioral Variations
However, differences occurred during instrumental responding tests. Junk-food fed obese-prone rats had reduced lever pressing compared with those fed chow, indicating diminished motivation to seek free food. Finally, following junk-food deprivation these obesity-prone rats showed increased lever pressing and other seeking behaviors for food which indicated enhanced motivation for food seeking purposes. Conversely, following withdrawal from junk food the obesity-resistant rats did not display significant changes in terms of their seeking behavior for meals.
Neural Mechanisms
Electrophysiological studies provided insights into the neural mechanisms underlying these behavioral changes. When junk-food was removed after it had caused obesity on craving a higher CP-AMPAR transmission was found within Nac but not in ors-rats (Li et al., 2016). This effect was specific for mPFC inputs but not those from BLA. Blocking activity in mPFC-to-NAc inputs using pharmacological inhibition or optogenetic techniques induced recruitment of CP-AMPARs in the nucleus accumbens of obesity-prone rats.
Implications for Obesity and Future Research
The analysis underscores the need to understand how diet-induced neural plasticity in reward circuits of the brain leads to obesity and offers multiple points of intervention when dealing with obesogenic diets.
“Such data adds to the mounting evidence that pre-disposition interacting with diet induced neurobehavioral plascticity is likely responsible for weight gain and maintenance of obesity,” states the researchers. This research highlights the importance of understanding what happens after a sugar and fat rich diet has been stopped permanently, which will lead to linking these changes in synapses with behavioral changes in future studies.
Conclusion
These findings reveal fresh insights into CP-AMPAR accrual within NAcc, involving putative mechanisms of synaptic scaling. This has important implications for both cue-triggered food- and potentially drug-seeking behaviors. By understanding these neural and behavioral alterations, scientists are optimistic about developing better ways of fighting against obesity as well as its health risks.
